Fig. (2).

Beneficial effects of eCB receptor activation in experimental models of neurological disease. A. In neurological pathologies such as Alzheimer’s and Parkinson’s disease, pathologic accumulation of misfolded or aggregated proteins (Amyloid β, α-synuclein, hyperphosphorylated Tau) promotes neuronal damage and development of inflammatory responses. In multiple sclerosis, aberrant recognition of self-antigens promotes demyelination and neuronal damage, causing CNS inflammation. Inflammatory responses in the CNS lead to activation of glial cells that produce proinflammatory mediators, promoting leukocyte recruitment and in some cases inducing differentiation of Th1 and Th17 cells that cause neuronal cell death. B. Activation of CB1 and CB2 receptors in leukocytes, glia and neurons prevent neuronal damage by decreasing classical microglial activation, improving the removal of myelin, decreasing the differentiation of Th1 and Th17 cells and promoting the differentiation of oligodendrocyte precursor cells (OPCs) to mature oligodendrocytes, improving remyelination and decreasing excitotoxic neuronal death. (Figure created by the authors). (A higher resolution / colour version of this figure is available in the electronic copy of the article).